LACK OF MAJOR HYPOXIA AND SIGNIFICANT BRAIN-DAMAGE IN RATS DESPITE DRAMATIC HYPONATREMIC ENCEPHALOPATHY

Brain myelinolysis could complicate the excessive correction of chroni c hyponatremia, Recently it was suggested that hypoxia rather than cor rection of hyponatremia would be responsible for myelinolysis. We anal yzed the Incidence and the severity of potentially associated hypoxia and its consequences on survival and on the development of brain damag e in rats in which major hyponatremic encephalopathy head developed af ter either pure acute hyponatremia (serum sodium concentration: -40 mE q/L/3 hr, group I, n = 8) or acute hyponatremia (serum sodium concentr ation: -30 mEq/L/3 hp, group II, n = 12) superimposed on chronic hypon atremia of 3 days' duration (serum sodium concentration: 113 mEq/L). O ur study revealed the following: (1) Despite dramatic hyponatremic enc ephalopathy (convulsions, coma, hypoxia (PO2 < 70 mm Hg) was present, but the PO2 was not decreased below 40 mm Hg. All of these rats died r apidly if they remained hyponatremic. (2) In the animals rescued by Na Cl, the incidence of brain myelinolysis was low (10%), whatever the du ration (pure acute or chronic plus acute) of the hyponatremia and desp ite the combination of hypoxia with major hyponatremic encephalopathy. (3) When acute hyponatremia is superimposed on a chronic preexisting hyponatremic state, the acute component of serum sodium concentration decrease could be rapidly corrected (serum sodium concentration: +35 m Eq/L/21 hr) without fear of permanent brain damage, Our results sugges t that even in the presence of dramatic hyponatremic encephalopathy an d associated hypoxia, neuropathologic sequelae are uncommon. Brain les ions related to post-anoxic encephalopathy probably develop only after respiratory arrest occurs.